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Calcium disorders: Treatment, symptoms, advice and help


Calcium is stored in the body almost exclusively in the bone. Only about 1% is available in the extra-cellular fluid. Most laboratories measure total serum calcium although the biologically active fraction is the ionised calcium. This accounts for about half the calcium measured.

The main binding protein for calcium within the serum is albumin. Calcium levels can appear low or high if the serum albumin is low or high. Formulae have been used to adjust for this. One formula commonly used is to add 0.02 mmol/L of calcium to the total calcium for every 1g/L that the serum albumin is below 40 and to subtract in the same way for every 1g/L that the albumin is above 40.

The result obtained gives an approximate estimate as to whether there is likely to be a normal amount of ionised calcium in the circulation. Ionised calcium is also affected by blood pH. Calcium disassociates from albumin in states of acidosis and binds in states of alkalosis. A mild tetany can be induced by hyperventilation.

Several hormones are involved in the regulation of calcium turnover of which the two most important are parathyroid hormone and 1, 25-dihydroxycholecalciferol.

Parathyroid Hormone

Parathyroid hormone is an 84 amino-acid polypetide secreted from the four parathyroid glands in response to the circulating calcium level mediated by a calcium receptor. The ultimate effect of parathyroid hormone within the bone is to stimulate osteoclast activity, bone breakdown and to release calcium into the circulation. In the kidneys it is a phosphaturic hormone and promotes calcium excretion. It stimulates the hydroxylation of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol in the kidneys.

Vitamin D

Vitamin D is a sterol which is synthesised in the skin as vitamin D3 (cholecalciferol). Vitamin D2 is used to fortify dairy products and is derived from a plant sterol. Vitamion D3 undergoes 25-hydroxylation to 25-hydroxycholecalicerol in the liver. It is converted in the kidneys to 1,25-dihydroxycholecalciferol, the active form, which promotes intestinal calcium absorption.


The two common causes of hypercalcaemia are primary hyperparathyroidism and malignancy. The relative frequency of each depends on the population surveyed. In community studies hyperparathyroidism is easily the most common cause. In hospital studies malignancy is more common.

Other causes of hypercalcaemia include thiazide diuretics, sarcoidosis, vitamin D intoxication, renal failure, milk alkali syndrome and familial hypocalciuric-hypercalaemia.

Symptoms Of Hypercalcaemiaa

In modern medical practice calcium is routinely measured as part of a biochemical profile. In consequence many more cases of hypercalcaemia come to light these days than in previous years. Most cases of hypercalcaemia are asymptomatic. More severe hypercalcaemia may cause tiredness, lethargy, thirst, polyuria, constipation and renal stones.


Primary hyperparathyroidism affects women more commonly than men. It most commonly arises from an adenoma in one of the four parathyroid glands. In the minority of cases there may be hyperplasia of all four glands. In a few cases there is also an association with multiple endocrine neoplasia.

The hypercalcaemia may be mild to severe and there is hypophosphataemia. Although not routinely measured 1,25-dihydroxycholecalciferol levels are raised due to stimulation of the renal 1-hydroxylation process by PTH. The adenoma may be localised by ultrasound scanning or sestamibi scanning. In practice the best way to localise an adenoma if this is necessary is at operation when performed by an experienced parathyroid surgeon.

In most cases the hyperparathy